This is phenomenal! I have spent hours sifting through papers trying to piece together the mechanism for the CFTR ion channel, and this was exactly the coherent explanation I needed. Thank you! Keep it up!
This video is absolutely excellent. I am a medical student writing my critical review dissertation project on CFTR modulators in the treatment of CF, and this video is a fantastic starter to understand the function of the CFTR channel under normal physiology. Thank you so much.
The EXACT peices of information I was looking for! Nowere else on the web has this level of specificity, comprehensibility and relativley about CFTR protein! Please take pride in this fact, you've earned it! :)
Very nice. Small correction: CFTR does not contain a PDZ domain, but a PDZ-interacting motif. This motif is the one that interacts with the PDZ domain of other proteins, including a cytoskeletal protein.
Congratulations on a very, very logical and systematic account. After seven years third level education in chemistry and pharmacology I can think of only one lecturer who came within an ass's roar of the explanation here. Very well done.
Its a deletion of phenylanine on the 508th amino acid. This receptor is made in the endoplasmic reticulum (ER) the deletion causes a slight misfold. Onces CFTR leaves the ER it is targeted for destruction due to misfolding. The ironic part of this mutation is that the receptor would most likely be functional even with this deletion; however, the cell is very "picky" and specific. Therefore, it destroys it instead of incorporating it into the membrane. Sorry for such a late response I am just stumbling upon this video. My cell biology is also a little rusty--grad school was over a year ago for me. This is how I remember it though.
This is phenomenal! I have spent hours sifting through papers trying to piece together the mechanism for the CFTR ion channel, and this was exactly the coherent explanation I needed. Thank you! Keep it up!
Damn. Why exactly has this channel not blown up yet? This channel is a treasure trove for anyone studying something medical related :D
This video is absolutely excellent. I am a medical student writing my critical review dissertation project on CFTR modulators in the treatment of CF, and this video is a fantastic starter to understand the function of the CFTR channel under normal physiology. Thank you so much.
The EXACT peices of information I was looking for! Nowere else on the web has this level of specificity, comprehensibility and relativley about CFTR protein! Please take pride in this fact, you've earned it! :)
Very nice. Small correction: CFTR does not contain a PDZ domain, but a PDZ-interacting motif. This motif is the one that interacts with the PDZ domain of other proteins, including a cytoskeletal protein.
Congratulations on a very, very logical and systematic account. After seven years third level education in chemistry and pharmacology I can think of only one lecturer who came within an ass's roar of the explanation here. Very well done.
This was absolutely amazing!!! Such a clear, concise explanation! Great job!!
Excellent video, you have made learning this so easy! Keep up the good work
Excellent! Love your videos. This is a professor of medicine talking'!
Beautifully done man. Got a clear concept Alhamdulillah.
An excellent show!!!
Brilliant video! Very clear explanation, thank you!
What a great synthesis! Thank you!
Allah razı olsun
Thanks for understanding everything patiently
Really good explanation!
This guy is a real deal!
Absolute genius !!
Thanks
Thank you!
thank you so much
Thankyou so so much !!
Beautifully explained, I had a doubt. How does hydrolysis occur? does the NBD-2 has ATPase property?
CFTR 680 Toronto.
i love this shiiittt XD
what mutation causes the channel to close thus resulting in chloride and sodium ions not be reabsorbed?
Its a deletion of phenylanine on the 508th amino acid. This receptor is made in the endoplasmic reticulum (ER) the deletion causes a slight misfold. Onces CFTR leaves the ER it is targeted for destruction due to misfolding.
The ironic part of this mutation is that the receptor would most likely be functional even with this deletion; however, the cell is very "picky" and specific. Therefore, it destroys it instead of incorporating it into the membrane.
Sorry for such a late response I am just stumbling upon this video. My cell biology is also a little rusty--grad school was over a year ago for me. This is how I remember it though.
I think i love you
Ii llikkee yoouuuu
Just realised how shit my teacher is